The MRSA superbug has an Achilles’ heel in the form of a gene that could be the target of new drug development, research shows.
The ftsH, picked out of 22 MRSA genes that help the bacterium cause disease, is considered to be a vulnerable spot. A team of British scientists have now found possible new roles for all of the 22 genes.
They produced a ‘gene map’ to raise their understanding of how MRSA develops resistance and were able, for the first time, to work out relationships between 95% of MRSA genes.
They also examined an antimicrobial agent called Ranalexin, derived from the skin of a bullfrog, which is able to kill MRSA. Computer analysis coupled with laboratory tests showed that the drug works by weakening the bacterial cell wall and membrane.
Dr Ian Overton, from the Medical Research Council Human Genetics Unit in Edinburgh, said: “Multidrug resistant Staphylococcal infections such as MRSA are a worldwide problem and strains resistant to existing treatments continue to emerge.
“The development of new drugs is therefore important. Our network biology approach has given insights into how Ranalexin works to kill MRSA and helped us to understand more about how infections may develop. This knowledge contributes towards new strategies for treating MRSA.”
The researchers included scientists at Edinburgh’s MRC Human Genetics Unit and the Universities of St Andrews, Dundee and London.
MRSA, methicillin resistant Staphylococcus aureus, is a mutant form of a common microbe which is immune to most antibiotics. In 2009 there were an estimated 781 deaths in the UK involving MRSA. Most MRSA infections happen in hospital due to the bug entering wounds.
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